Browsing by Author "Okesina, A. A."

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    Activation of pro-apoptotic cells, reactive astrogliosis and hyperphosphorylation of tau protein in trimethyltin-induced hippocampal injury in rats
    (Association of Anatomical Societies of Africa, 2020) Okesina, A. A.; Ajao, M. S.; Buhari, M. O.; Afodun, A. M.; Okesina, K. B.; Usman, R. Y.; Sulaimon, F. A.,
    Neurodegenerative diseases cause neural cells to lose both the functional and sensory abilities as a result of genetic factors, proteopathies and mitochondrial dysfunction. Neurodegeneration forms the basis of most neurodegenerative disorders for example Alzheimer’s disease, Huntington’s diseases, and Parkinson’s diseases. The mechanism that underlines the process of neurodegeneration is not well understood. Understanding the process and mechanism involved in neurodegeneration might offer a better therapeutic approach to positively manage cases of neurodegenerative diseases. Therefore, this study’s target was to create an animal model to study neurodegeneration. Sixteen adult male Wistar rats were used in the study and divided into two groups. Control (0.2 mL of normal saline (NS)), and trimethyltin-treated (TMT, 8 mg/kg stat dose only). These animals underwent perfusion with 4% paraformaldehyde, brain excision and analysis of p53 antigen, GFAP and Bielshowsky on these tissues. The results showed that animals in the control group showed presence of activated p53 antigen, reactive astrogliosis, neurofibrillary tangles, and amyloid plaques within the cytoplasm of the hippocampal cells. Cornus Ammonis (CA2) and (CA3) showed more of the trimethylrtin injury than CA1 and CA4. This study thus revealed that, intra-peritoneal administration of single dose of 8mg/kg of trimethyltin can offer an attractive disease model to study some neurodegenerative diseases.
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    Exogenous melatonin restored the cytoarchitectural integrity and biochemical activities of the cerebrum in sodium fluoride-induced toxicity.
    (Spanish Society of Anatomy and the Mexican Society of Anatomy, 2021) Ibrahim-Abdulkareem, R. A.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Yawson, E.; Oluyomi, O.O.; Ajao M.S
    The cerebrum is responsible for motor, sensory and autonomic activities of the human body, and it is believed that fluoride exposure to the biological system can impede these functions. Therefore, it is imperative to introduce melatonin to limit the extent of fluoride toxicity on the cerebrum and understand the mechanism involved in the aforementioned process. Thirty-two rats were randomly selected into 4 groups (n=8, per group). Groups I-IV received oral administration of 0.2ml of normal saline (NS), 500ppm of sodium fluoride (NaF), concurrent administration of sodium fluoride and melatonin (NaF+MLT), and sodium fluoride before melatonin (NaF-MLT) for fourteen days respectively. At the end of these treatments, the rats were euthanized and cerebral tissues were excised for histological, histochemical and biochemical analyses. Sodium fluoride distorted the shapes and size of the cells and caused constriction of the blood vessels, as well as presence of vacuolations in the cells of the pyramidal layer of the cerebral cortex. However, melatonin was able to restore the cytoarchitecture of cells of the pyramidal layer of the cerebral cortex when administered concurrently and after the administration of sodium fluoride (NaF) respectively. Also, melatonin regulated the activities of Superoxide dismutase, Malondialdehyde and Glutathione peroxidase in the cerebrum. Sodium fluoride causes neurodegeneration in the cerebral cortex, and exogenous melatonin can ameliorate the injury caused by sodium fluoride on the cerebral cortex.
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    Nigella sativa oil ingestion mitigates aluminum chloride (alcl3) induced cerebellar oxidative, neurogenic damages and impaired motor functions in Wistar rats
    (Association of Anatomical Societies of Africa, 2022) Imam, A.; Sulaimon, F. A.; Shehu, M.; Busari, M.; Oyegbola, C.; Okesina, A. A.; Afodun A. M.; Adana, M. Y.; Ajao, M. S.
    Varying neurological effects, and impairments to motor functions, neurochemistry and neuromorphology have been associated with Aluminium chloride (AlCl3) induced neurotoxicity. This study aims to investigate the efficacy of Nigella sativa oil (NSO) in AlCl3 induced cerebellar toxicity in rats. Thirty-two male Wistar rats were randomly divided into four groups and received: normal saline; 100 mg/kg.bw of AlCl3; 100 mg/kg.bw AlCl3 and 1 ml/kg.bw of NSO; and 1 ml/kg.bw, orally and daily for fourteen days. On the 13th day of the experiment, the rats were each exposed to a single trial of the Open Field Test (OFT), of which line crossing frequency, rearing frequency, and freezing period were recorded as measures of exploratory and locomotive behaviours of the animals. By day 15, the rats were euthanized, their brains were excised, the cerebellum dissected from five brains of each group, and homogenized for biochemical evaluations of nitric oxide (NO) metabolites and total reactive oxygen species (ROS) levels. The remaining three brains in each group were processed for histology and Ki67 immunohistochemistry investigations. The results of this study shows that AlCl3 impaired motor related behaviours in the AlCl3 exposed animals, by significantly reducing the line crossing and rearing frequencies, and increasing the freezing period. This effect was observed to be mitigated in the animal group that received NSO following AlCl3 administration, as the animals showed improved motor behaviours. AlCl3 also caused an increase in the cerebellar activities of NO and ROS, while it depleted Ki67 expressions and caused neurodegenerative-like effects in the cerebellar histoarchitecture of the exposed animals. Intervention with NSO depleted ROS/NO levels and protected the cerebellum from the nitrosative and oxidative stress induced by AlCl3. NSO was also observed to preserve the cerebellar cortex histoarchitecture and neurogenic morphology against the neurodegenerative effect of AlCl3. It can be concluded that NSO, with its high efficacy against oxidative stress and neuroinflammation, is a potent natural therapeutic agent in aluminum and heavy metal neurotoxicity.
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    Phoenix dactylifera polyphenols ameliorates monosodium glutamate induced cell damage in the dentate gyrus
    (Krishna Institute of Medical Sciences, 2021) Usman, R. Y.; Sulaimon, F. A.; Okesina, A. A.; Imam, A.; Imam, A. L.; Ajao M. S
    Background: Monosodium Glutamate (MSG) use is quite alarming considering the cascades of toxicity that arises from it. However, this study demonstrated the possible ameliorative activities of polyphenols of Phoenix dactylifera (PPD) on MSG-induced dentate gyrus degeneration in male adult Wistar rats. Aim and Objectives: To check the effects of PPD on MSG induced dentate gyrus neuronal damage in adult male Wistar rats. Material and Methods: Groups A to D of adult male rats underwent 14-day treatment of Normal Saline (NS), 500 mg ̸ kg PPD, 4 mg ̸g of MSG only, and 4 mg̸g MSG and 500 mg/kg PPD (MSG+PPD) concurrently. Group E received 500 mg ̸ kg PPD for a 14-day period prior to another 14-day of 4mg ̸ gMSG (PPD then MSG). Results: PPD was able to ameliorate the toxic effect of MSG as evidence of better cellular integrity, minimal cell vacuolations, minimized dispersed Nissl bodies and deeply stained Nissl bodies were observed upon PPD administration. It was also observed that it reduced the proliferation of reactive oxygen species, proteins and DNAdamage in the cells of the dentate gyrus. Conclusion: The study concluded that PPD was able to ameliorate the degeneration induced by MSG in the dentate gyrus of Wistar rats
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    Thymoquinone ameliorate oxidative stress, GABAergic neuronal depletion and memory impairment through Nrf2/ARE signaling pathway in the dentate gyrus following cypermethrin administration
    (BMC Neuroscience, 2024) Imam, A. L.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Ibiyeye, R. Y.; Oyewole, L. A.; Biliaminu, S. A.; Shehu, M.; Alli, A. O.; Omoola, O. O.; Ajao, M.S.
    Background Exposure to chemical toxins, including insecticides, harms bodily organs like the brain. This study examined the neuroprotective of thymoquinone on the cypermethrin’s harmful effects on the histoarchitecture of the dentate gyrus and motor deficit in the dentate gyrus. Methods Forty adult male rats (180–200 g) were randomly divided into 5 groups (n=8 per group). Groups I, II, III, IV, and V received oral administration of 0.5 ml of phosphate-buffered saline, cypermethrin (20 mg/kg), thymoquinone (10 mg/kg), cypermethrin (20 mg/kg)+thymoquinone (5 mg/kg), and cypermethrin (20 mg/kg)+thymoquinone (10 mg/kg) for 14 days respectively. The novel object recognition test that assesses intermediate-term memory was done on days 14 and 21 of the experiment. At the end of these treatments, the animals were euthanized and taken for cytoarchitectural (hematoxylin and eosin; Cresyl violet) and immunohistochemical studies (Nuclear factor erythroid 2-related factor 2 (Nrf2), Parvalbumin, and B-cell lymphoma 2 (Bcl2). Result The study shows that thymoquinone at 5 and 10 mg/kg improved Novelty preference and discrimination index. Thymoquinone enhanced Nissl body integrity, increased GABBAergic interneuron expression, nuclear factor erythroid 2-derived factor 2, and enhanced Bcl-2 expression in the dentate gyrus. It also improved the concentration of nuclear factor erythroid 2-derived factor 2, increased the activities of superoxide dismutase and glutathione, and decreased the concentration of malondialdehyde level against cypermethrin-induced neurotoxicity. Conclusion thymoquinone could be a therapeutic agent against cypermethrin poisoning.
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    Thymoquinone Ingestions Reversed Inflammation Driven Glia activation and Impaired Cognitive associated behavior in Cypermethrin Exposed Rats.
    (Uskudar University, 2024) Imam, A. L.; Okesina, A. A.; Sulaimon, F. A.; Imam, A.; Ibiyeye, R. Y.; Adana, M. Y.; Omoola, O. O.; Ajao, M. S.
    Background: Pyrethroids pose health risks to humans. Therefore, it is imperative to assess the preventive benefits of thymoquinone against neurotoxicity induced by cypermethrin- in the hippocampal dentate gyrus. Methods: Forty male adult Wistar rats with an average weight of 180-200g were randomly allocated to five (5) groups, and each comprising eight rats (n=8 per group). The groups were designated as follows, through oral administrations for 14 days: 0.5ml phosphate- buffered saline (PBS) was given to group one; Group two received 20mg/kg of cypermethrin (CYM); Group three received 10 mg/kg of thymoquinone (THQ); Group four received 20 mg/kg of cypermethrin followed by 10mg/kg of thymoquinone (CYM-10mgTHQ); and Group five received 20mg/kg and 5mg/kg cypermethrin and thymoquinone respectively (CYM-5mgTHQ). Behavioral, histological, immunohistochemical, and biochemical analyses were conducted post-treatment. Results: Cypermethrin administration caused the rise in pro-inflammatory cytokine TNF-α and increased expression of astrocytes, microglia, and pro-apoptotic protein Bax. Additionally, cypermethrin reduced levels of anti-inflammatory cytokine IL-10, acetylcholinesterase (AChE) activity, and nuclear factor erythroid 2-related factor 2 (Nrf2). cytoarchitectural disruption of dentate gyrus and decreased Nrf2 expression were observed. Cognitive deficits were evident. Thymoquinone treatment attenuated TNF-α elevation, reduced astrocyte, microglial, and Bax expression, and increased IL-10, AChE, and Nrf2 levels. Conclusion: Thymoquinone demonstrated anti-inflammatory and anti-apoptotic effects against cypermethrin-induced neurotoxicity, improving cognitive function in rats.